Artykuły w czasopismach: „Pulmonary arterial hyperreactivity”

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Cardouat, G., M. Douard, L. Roubenne, C. Bouchet, Z. Kmecová, P. Robillard, C. Guignabert i in. "NGF induces pulmonary arterial hyperreactivity through Connexin 43 increased expression". Revue des Maladies Respiratoires 38, nr 6 (czerwiec 2021): 582. http://dx.doi.org/10.1016/j.rmr.2021.02.029.

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Cardouat, G., M. Douard, L. Roubenne, S. Kmecova, P. Robillard, C. Guignabert, L. Tu i in. "NGF induces pulmonary arterial hyperreactivity through Connexin 43 increased expression". Archives of Cardiovascular Diseases Supplements 12, nr 2-4 (październik 2020): 213. http://dx.doi.org/10.1016/j.acvdsp.2020.03.036.

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Bouchet, Clement, Guillaume Cardouat, Matthieu Douard, Paul Robillard, Roger Marthan, Christelle Guibert i Véronique Freund-Michel. "Short-term mechanisms activated by NGF to induce pulmonary arterial hyperreactivity". Archives of Cardiovascular Diseases Supplements 14, nr 2 (czerwiec 2022): 157–58. http://dx.doi.org/10.1016/j.acvdsp.2022.04.147.

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Bouchet, C., G. Cardouart, M. Douard, Z. Kmecova, P. Robillard, F. Delcambre, R. Marthan, P. Berger, C. Guibert i V. Freund-Michel. "Short-term mechanisms activated by NGF to induce pulmonary arterial hyperreactivity". Revue des Maladies Respiratoires 40, nr 2 (luty 2023): 129. http://dx.doi.org/10.1016/j.rmr.2022.11.041.

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Hinton, M., L. Mellow, A. J. Halayko, A. Gutsol i S. Dakshinamurti. "Hypoxia induces hypersensitivity and hyperreactivity to thromboxane receptor agonist in neonatal pulmonary arterial myocytes". American Journal of Physiology-Lung Cellular and Molecular Physiology 290, nr 2 (luty 2006): L375—L384. http://dx.doi.org/10.1152/ajplung.00307.2005.

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PPHN, caused by perinatal hypoxia or inflammation, is characterized by an increased thromboxane-prostacyclin ratio and pulmonary vasoconstriction. We examined effects of hypoxia on myocyte thromboxane responsiveness. Myocytes from 3rd–6th generation pulmonary arteries of newborn piglets were grown to confluence and synchronized in contractile phenotype by serum deprivation. On the final 3 days of culture, myocytes were exposed to 10% O2 for 3 days; control myocytes from normoxic piglets were cultured in 21% O2. PPHN was induced in newborn piglets by 3-day hypoxic exposure (FiO2 0.10); pulmonary arterial myocytes from these animals were maintained in normoxia. Ca2+ mobilization to thromboxane mimetic U-46619 and ATP was quantified using fura-2 AM. Three-day hypoxic exposure in vitro results in increased basal [Ca2+]i, faster and heightened peak Ca2+ response, and decreased U-46619 EC50. These functional changes persist in myocytes exposed to hypoxia in vivo but cultured in 21% O2. Blockade of Ca2+ entry and store refilling do not alter peak U-46619 Ca2+ responses in hypoxic or normoxic myocytes. Blockade of ryanodine-sensitive or IP3-gated intracellular Ca2+ channels inhibits hypoxic augmentation of peak U-46619 response. Ca2+ response to ryanodine alone is undetectable; ATP-induced Ca2+ mobilization is unaltered by hypoxia, suggesting no independent increase in ryanodine-sensitive or IP3-linked intracellular Ca2+ pool mobilization. We conclude hypoxia has a priming effect on neonatal pulmonary arterial myocytes, resulting in increased resting Ca2+, thromboxane hypersensitivity, and hyperreactivity. We postulate that hypoxia increases agonist-induced TP-R-linked IP3 pathway activation. Myocyte thromboxane hyperresponsiveness persists in culture after removal from the initiating hypoxic stimulus, suggesting altered gene expression.

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Peták, Ferenc, Tibor Z. Janosi, Carole Myers, Fabienne Fontao i Walid Habre. "Impact of elevated pulmonary blood flow and capillary pressure on lung responsiveness". Journal of Applied Physiology 107, nr 3 (wrzesień 2009): 780–86. http://dx.doi.org/10.1152/japplphysiol.00157.2009.

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Since alterations in pulmonary hemodynamics may lead to airway hyperreactivity, the consequences of individual changes in pulmonary blood flow (Q̇p) and capillary pressure (Pc) on lung responsiveness were investigated. During maintenance of a steady-state Pc of 5, 10, or 15 mmHg ( groups 1–3), acute increases of Q̇p were generated in isolated, perfused rat lungs by simultaneous pulmonary arterial pressure elevation and venous pressure lowering. Conversely, at constant low ( groups 4 and 5) or high Q̇p ( groups 6 and 7), Pc was lowered or elevated by changing, in parallel, the pulmonary arterial and venous pressures. Pulmonary input impedance was measured under baseline conditions and during methacholine provocation (2–18 μg·kg−1·min−1), whereas the pulmonary hemodynamics were altered in accordance with the group allocation. The airway resistance and constant-phase parenchymal model parameters were identified from the pulmonary input impedance spectra. Increases of Q̇p at constant Pc had no effect on the basal lung mechanics, whereas they enhanced the lung reactivity to methacholine, particularly when high Pc was maintained [peak airway resistance increases of 299 ± 99% (SE) vs. 609 ± 217% at Q̇p levels of 5 and 10 ml/min, respectively, P < 0.05]. In contrast, the change of Pc at constant Q̇p slightly deteriorated the basal parenchymal mechanics without affecting the lung responsiveness. These findings suggest that increases in Q̇p per se may lead to the development of airway hyperreactivity. This phenomenon may contribute to the airway susceptibility under conditions associated with simultaneous elevations in pulmonary vascular pressures and Q̇p, such as exercise-induced asthma and the situation in children with congenital heart diseases.

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Smith, Kelly J., George B. Mallory, Steven H. Abman i Dunbar D. Ivy. "AIRWAY HYPERREACTIVITY AFTER ILOPROST INHALATION IN PEDIATRIC PATIENTS WITH PULMONARY ARTERIAL HYPERTENSION". Chest 130, nr 4 (październik 2006): 156S. http://dx.doi.org/10.1378/chest.130.4_meetingabstracts.156s-b.

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Michel, R. P., i T. S. Hakim. "Increased resistance in postobstructive pulmonary vasculopathy: structure-function relationships". Journal of Applied Physiology 71, nr 2 (1.08.1991): 601–10. http://dx.doi.org/10.1152/jappl.1991.71.2.601.

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Postobstructive pulmonary vasculopathy (POPV) was produced by chronic ligation (120 days) of the left main pulmonary artery of seven dogs. To explain the abnormal physiological changes found using arterial and venous occlusion (AVO) in POPV (J. Appl. Physiol. 69: 1022–1032, 1990), the light-microscopic morphology, morphometry (n = 5), and ultrastructure (n = 6) of ligated left lower lobes were compared with contralateral control right lower lobes. First, there was a proliferation of bronchial vessels around pulmonary vessels and airways to explain bronchial blood flow rates of 330 ml/min in left lower lobes. The walls of the bronchial vessels contained smooth muscle with minimal elastic tissue and prominent myoendothelial junctions. Second, focal bronchopulmonary anastomoses were seen in pulmonary arteries approximately equal to 100 microns diam, which is consistent with our conclusion that the major site of communication is at the precapillary level and suggests that the limit between arterial and middle segments defined by AVO may lie in arteries of approximately equal to 100 microns. Third, to explain the increased arterial resistance in POPV, the pulmonary arteries had an increased percent medial muscle thickness, peripheral muscularization, and focal intimal thickening but had no plexiform lesions. The ultrastructure of the arteries revealed new intimal cells and numerous myoendothelial junctions rarely found in controls. Capillaries and veins were only subtly altered. Fourth, the hyperreactivity of arteries to serotonin and of veins to histamine found using AVO was partially explained by the increased medial thickness and decreased diameter but may also be due to increased receptor concentration or related to the myoendothelial junctions. We conclude that most of the hemodynamic alterations in POPV are related to morphological abnormalities and that this model has clinical and experimental relevance in the study of bronchopulmonary vascular interactions.

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Azamar-Solis, Brizeida, Yahveth Cantero-Fortiz, Juan Carlos Olivares-Gazca, Jesús Mauricio Olivares-Gazca, Gisela Berenice Gómez-Cruz, Iván Murrieta-Álvarez, Guillermo J. Ruiz-Delgado i Guillermo J. Ruiz-Argüelles. "Primary Thrombophilia in Mexico XIII: Localization of the Thrombotic Events in Mexican Mestizos With the Sticky Platelet Syndrome". Clinical and Applied Thrombosis/Hemostasis 25 (1.01.2019): 107602961984170. http://dx.doi.org/10.1177/1076029619841700.

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The sticky platelet syndrome (SPS) is a common cause of both arterial and venous thrombosis, being a dominant autosomal disease with qualitative platelet alterations and familial occurrence. It is characterized by platelet hyperreactivity with increased platelet aggregability in response to low concentrations of platelet agonists: epinephrine, adenosine diphosphate, or both. The clinical manifestations involve venous or arterial thrombosis, recurrent pregnancy loss, and fetal growth retardation. To analyze the localization of the thrombotic episodes in a cohort of Mexican mestizo patients with SPS. Between 1992 and 2016, 86 Mexican mestizo patients with SPS as the single thrombophilic condition were prospectively identified; all of them had a history of thrombosis. There were 15 males and 71 females. The thrombotic episodes were arterial in 26 cases and venous in 60 (70%). Arterial thrombosis was mainly pulmonary thromboembolism, whereas venous thromboses were identified most frequently in the lower limbs. Mexican mestizo population with SPS is mainly female; the type I of the condition is the most frequent; both arterial and venous thrombosis can occur, and they are mainly pulmonary embolism and lower limbs venous thrombosis, respectively.

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Ohar, Jill A., Kemberly S. Waller i Thomas E. Dahms. "Platelet-activating Factor Induces Selective Pulmonary Arterial Hyperreactivity in Isolated Perfused Rabbit Lungs". American Review of Respiratory Disease 148, nr 1 (lipiec 1993): 158–63. http://dx.doi.org/10.1164/ajrccm/148.1.158.

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Morley, J., S. Sanjar i C. Newth. "Viewpoint: untoward effects of beta-adrenoceptor agonists in asthma". European Respiratory Journal 3, nr 2 (1.02.1990): 228–33. http://dx.doi.org/10.1183/09031936.93.03020228.

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Beta-adrenoceptor agonists are potent and selective relaxants of airway smooth muscle. They produce symptomatic bronchodilatory effects and are the most widely used therapy in asthma. In patients with asthma, they usually effect a reduction of airway resistance, but there have been several reports of episodes of increased airway obstruction, arterial hypoxaemia and even death associated with such therapy. "Anomalous or paradoxical bronchospasm" are appropriate terminologies to describe this unexpected phenomenon. Five mechanisms have been proposed to account for anomalous responses to these substances: 1) reactive myogenic tone; 2) metabolic products with spasmogenic activity; 3) adrenoceptor tachyphylaxis; 4) increased inflammatory burden; and 5) induction of airway hyperreactivity. Following a review of the relative merits of each proposal, it is concluded that increased inflammatory burden and induction of airway hyperreactivity, alone or in combination, provide the most plausible explanation for paradoxical bronchospasm.

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Hiram, Roddy, Edmond Rizcallah, Sofia Marouan, Chantal Sirois, Marco Sirois, Caroline Morin, Samuel Fortin i Eric Rousseau. "Resolvin E1 normalizes contractility, Ca2+ sensitivity and smooth muscle cell migration rate in TNF-α- and IL-6-pretreated human pulmonary arteries". American Journal of Physiology-Lung Cellular and Molecular Physiology 309, nr 8 (15.10.2015): L776—L788. http://dx.doi.org/10.1152/ajplung.00177.2015.

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Pulmonary hypertension (PH) is a rare disease in which pathophysiology is characterized by an increase in proinflammatory mediators, chronic endothelial dysfunctions, and a high migration rate of smooth muscle cells (SMC). Over the course of the last decade, various treatments have been proposed to relax the pulmonary arteries, none of which have been effective in resolving PH. Our hypothesis is that artery-relaxing drugs are not the long-term solution, but rather the inhibition of tissue inflammation, which underlies human pulmonary artery (HPA) dysfunctions that lead to abnormal vasoconstriction. The goal of the present study was to assess the anti-inflammatory effects of resolvin E1 (RvE1) with concomitant effects on SMC migration and on HPA reactivity. The role and mode of action of RvE1 and its precursor, monoacylglyceride eicosapentaenoic acid were assessed on HPA under proinflammatory conditions, involving a combined pretreatment with 10 ng/ml TNF-α and 10 ng/ml IL-6. Our results show that TNF-α and IL-6 treatment induced hyperreactivity and Ca2+ hypersensitivity in response to pharmaco-mechanical stimuli, including 80 mM KCl, 1 μM phorbol 12–13-dibutyrate, and 30 nM U-46619. Furthermore, the proinflammatory treatment increased the migration rate of SMC isolated from HPA. The phosphorylation level of regulatory contractile proteins (CPI-17, MYPT-1), and proinflammatory signaling pathways (c-Fos, c-Jun, NF-κB) were also significantly increased compared with control conditions. Conversely, 300 nM RvE1 was able to normalize all of the above abnormal events triggered by proinflammation. In conclusion, RvE1 can resolve human arterial hyperreactivity via the resolution of inflammatory markers.

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TAKENAKA, TAKASHI, YUJI OGAWA i KATSUYUKI TOBISE. "Ca2+-induced contraction and hyperreactivity of pulmonary arterial smooth muscle in monocrotaline-treated rats." Japanese Circulation Journal 54, nr 5 (1990): 515–23. http://dx.doi.org/10.1253/jcj.54.515.

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Cardouat, Guillaume, Matthieu Douard, Clément Bouchet, Lukas Roubenne, Zuzana Kmecová, Pauline Esteves, Fabien Brette i in. "NGF increases Connexin-43 expression and function in pulmonary arterial smooth muscle cells to induce pulmonary artery hyperreactivity". Biomedicine & Pharmacotherapy 174 (maj 2024): 116552. http://dx.doi.org/10.1016/j.biopha.2024.116552.

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Cardouat, G., M. Douard, C. Bouchet, Z. Kmecová, P. Robillard, F. Delcambre, R. Marthan, B. Muller, C. Guibert i V. Freund-Michel. "Short-term mechanisms activated by the nerve growth factor NGF to induce pulmonary arterial hyperreactivity". Revue des Maladies Respiratoires 39, nr 2 (luty 2022): 120. http://dx.doi.org/10.1016/j.rmr.2022.02.029.

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Cardouat, G., M. Douard, P. Robillard, M. Dubois, R. Marthan, B. Muller, C. Guibert i V. Freund-Michel. "Short-term mechanisms activated by the nerve growth factor NGF to induce pulmonary arterial hyperreactivity". Archives of Cardiovascular Diseases Supplements 11, nr 2 (kwiecień 2019): 202. http://dx.doi.org/10.1016/j.acvdsp.2019.02.045.

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Reyes, R. V., E. A. Herrera, G. Ebensperger, E. M. Sanhueza, D. A. Giussani i A. J. Llanos. "Perinatal cardiopulmonary adaptation to the thin air of the Alto Andino by a native Altiplano dweller, the llama". Journal of Applied Physiology 129, nr 1 (1.07.2020): 152–61. http://dx.doi.org/10.1152/japplphysiol.00800.2019.

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Most mammals have a poor tolerance to hypoxia, and prolonged O2 restriction can lead to organ injury, particularly during fetal and early postnatal life. Nevertheless, the llama ( Lama Glama) has evolved efficient mechanisms to adapt to acute and chronic perinatal hypoxia. One striking adaptation is the marked peripheral vasoconstriction measured in the llama fetus in response to acute hypoxia, which allows efficient redistribution of cardiac output toward the fetal heart and adrenal glands. This strong peripheral vasoconstrictor tone is triggered by a carotid body reflex and critically depends on α-adrenergic signaling. A second adaptation is the ability of the llama fetus to protect its brain against hypoxic damage. During hypoxia, in the llama fetus there is no significant increase in brain blood flow. Instead, there is a fall in brain O2 consumption and temperature, together with a decrease of Na+-K+-ATPase activity and Na+ channels expression, protecting against seizures and neuronal death. Finally, the newborn llama does not develop pulmonary hypertension in response to chronic hypoxia. In addition to maintaining basal pulmonary arterial pressure at normal levels the pulmonary arterial pressor response to acute hypoxia is lower in highland than in lowland llamas. The protection against hypoxic pulmonary arterial hypertension and pulmonary contractile hyperreactivity is partly due to increased hemoxygenase-carbon monoxide signaling and decreased Ca2+ sensitization in the newborn llama pulmonary vasculature. These three striking physiological adaptations of the llama allow this species to live and thrive under the chronic influence of the hypobaric hypoxia of life at high altitude.

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Callejo, Maria, Gema Mondejar-Parreño, Daniel Morales-Cano, Bianca Barreira, Sergio Esquivel-Ruiz, Miguel Angel Olivencia, Grégoire Manaud i in. "Vitamin D deficiency downregulates TASK-1 channels and induces pulmonary vascular dysfunction". American Journal of Physiology-Lung Cellular and Molecular Physiology 319, nr 4 (1.10.2020): L627—L640. http://dx.doi.org/10.1152/ajplung.00475.2019.

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Vitamin D (VitD) receptor regulates the expression of several genes involved in signaling pathways affected in pulmonary hypertension (PH). VitD deficiency is highly prevalent in PH, and low levels are associated with poor prognosis. We investigated if VitD deficiency may predispose to or exacerbate PH. Male Wistar rats were fed with a standard or a VitD-free diet for 5 wk. Next, rats were further divided into controls or PH, which was induced by a single dose of Su-5416 (20 mg/kg) and exposure to hypoxia (10% O2) for 2 wk. VitD deficiency had no effect on pulmonary pressure in normoxic rats, indicating that, by itself, it does not trigger PH. However, it induced several moderate but significant changes characteristic of PH in the pulmonary arteries, such as increased muscularization, endothelial dysfunction, increased survivin, and reduced bone morphogenetic protein ( Bmp) 4, Bmp6, DNA damage-inducible transcript 4, and K+ two - pore domain channel subfamily K member 3 ( Kcnk3) expression. Myocytes isolated from pulmonary arteries from VitD-deficient rats had a reduced whole voltage-dependent potassium current density and acid-sensitive (TASK-like) potassium currents. In rats with PH induced by Su-5416 plus hypoxia, VitD-free diet induced a modest increase in pulmonary pressure, worsened endothelial function, increased the hyperreactivity to serotonin, arterial muscularization, decreased total and TASK-1 potassium currents, and further depolarized the pulmonary artery smooth muscle cell membrane. In human pulmonary artery smooth muscle cells from controls and patients with PH, the active form of VitD calcitriol significantly increased KCNK3 mRNA expression. Altogether, these data strongly suggest that the deficit in VitD induces pulmonary vascular dysfunction.

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Cardouat, G., M. Douard, P. Robillard, M. Dubois, R. Marthan, B. Muller, C. Guibert, V. Freund-Michel i Z. Kmecová. "Role of Connexin 43 increased expression in pulmonary arterial hyperreactivity induced by the nerve growth factor NGF". Archives of Cardiovascular Diseases Supplements 11, nr 2 (kwiecień 2019): 203. http://dx.doi.org/10.1016/j.acvdsp.2019.02.048.

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Clini, V., G. Pozzi i A. Ferrara. "Bronchial Hyperreactivity and Arterial Carboxyhemoglobin as Detectors of Air Pollution in Milan: A Study on Normal Subjects". Respiration 47, nr 1 (1985): 1–10. http://dx.doi.org/10.1159/000194742.

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Villagra, Jose D., James T. Nichols, Mark T. Gladwin i Gregory J. Kato. "Platelets from Patients with Sickle Cell Disease and Pulmonary Arterial Hypertension Are Hypersensitive to Agonist-Induced Activation." Blood 108, nr 11 (16.11.2006): 1239. http://dx.doi.org/10.1182/blood.v108.11.1239.1239.

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Abstract Pulmonary arterial hypertension (PAH) in sickle cell disease (SCD) is associated with chronic hemolysis and nitric oxide (NO) consumption and characterized by abnormal vascular tone, vascular proliferation and thrombosis. In previous studies, we demonstrated that increased platelet activation is linked to the severity of PAH in SCD. In addition, we reported that patients with SCD and secondary PAH have decreased platelet activation when given sildenafil, a finding that highlights the role of nitric oxide inhibition by hemolysis in this pathological mechanism. Since the vascular homeostasis is altered by the release of hemoglobin in plasma, we hypothesized that platelets of patients with PAH may show an enhanced degree of reactivity to platelet agonists released during hemolysis. Whole-blood samples were used to determine the in vivo baseline and stimulated platelet activation from SCD patients with PAH, without PAH during steady state (not in pain crisis) and healthy controls. PAH was defined by a tricuspid regurgitant jet velocity ≥ 2.5 m/sec by Doppler echocardiography. Upon withdrawal, citrated venous whole blood was mixed gently with either phosphate-buffered saline (PBS) or escalating doses (1 – 10 μM final concentration) of adenosine diphosphate (ADP), a platelet agonist present in red blood cells. Platelet activation was measured by the flow cytometry detection of activated fibrinogen receptors (activated GPIIb/IIIa) and surface expression of P-selectin. Patients with SCD and PAH reached high degrees of activation with significantly lower concentrations of ADP (EC50 0.88 μM, 95% confidence interval 0.64 to 1.23, n=5) compared to controls (1.3 μM, 1.00 to 1.64, p < 0.01, n=8), and particularly to patients without PAH (1.7μM, 1.31 to 2.27, n=5)(Figure below, left panel). Similar results were observed in parallel experiments with thrombin-receptor activating peptide, another strong platelet agonist. In separate experiments on platelets from healthy subjects, the addition of cell-free plasma hemoglobin induced platelet activation in dose-dependent fashion (p<0.05), supporting intravascular hemolysis as a mechanism of platelet activation in SCD (Figure below, right panel). Furthermore, cell-free hemoglobin blocked the ex vivo platelet inhibitory effects of an exogenous NO donor, MAHMANONOate (p<0.05), consistent with NO scavenging by cell-free hemoglobin. These findings suggest that platelets from patients with SCD and PAH are unusually sensitive to activation. Our data also suggests that most of the variability in platelet hyperreactivity observed by other groups in SCD is primarily associated with PAH. Our data support a role for intravascular hemolysis and NO scavenging by cell-free hemoglobin in platelet hyperreactivity. Additional research is needed to define this mechanistic pathway in more detail. Figure Figure

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Derksen, F. J., N. E. Robinson, P. J. Armstrong, J. A. Stick i R. F. Slocombe. "Airway reactivity in ponies with recurrent airway obstruction (heaves)". Journal of Applied Physiology 58, nr 2 (1.02.1985): 598–604. http://dx.doi.org/10.1152/jappl.1985.58.2.598.

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We measured lung function and airway reactivity to histamine administered by aerosol in two groups of ponies. Principal ponies had a history of heaves, a disease characterized by recurrent airway obstruction when ponies are housed in a barn and fed hay; control ponies had no history of airway obstruction. Ponies were paired (principal and control) and measurements were made when principal ponies were at pasture and in clinical remission (period A), following barn housing when principal ponies had acute airway obstruction (period B), and after a further 1 and 2 wk at pasture (periods C and D). At periods A, C, and D dynamic compliance (Cdyn), pulmonary resistance (RL), arterial O2 tension (PaO2), and CO2 tension (PaCO2) of principals and controls did not differ. Barn housing (period B) decreased Cdyn and PaO2 and increased RL in principals but not controls. The ED65Cdyn (the dose of histamine to reduce Cdyn to 65% of base line) did not differ in principals and controls at periods A, C, and D. At period B, ED65Cdyn decreased by 2.5-log doses of histamine in principals while ED65Cdyn was not affected in controls. There was no correlation between changes in airway reactivity and changes in RL and Cdyn. We conclude that ponies in clinical remission from heaves are not hyperreactive to histamine aerosol. This model of lung disease is similar to some forms of industrial asthma in which hyperreactivity occurs only during acute airway obstruction. The lack of correlation between ED65Cdyn and the degree of airway obstruction suggests that the hyperreactivity of principal ponies to histamine aerosol cannot be explained solely by alterations in baseline airway caliber.

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Habre, Walid, Tibor Z. Jánosi, Fabienne Fontao, Carole Meyers, Gergely Albu, Jean-Claude Pache i Ferenc Peták. "Mechanisms for lung function impairment and airway hyperresponsiveness following chronic hypoxia in rats". American Journal of Physiology-Lung Cellular and Molecular Physiology 298, nr 4 (kwiecień 2010): L607—L614. http://dx.doi.org/10.1152/ajplung.00222.2009.

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Although chronic normobaric hypoxia (CH) alters lung function, its potential to induce bronchial hyperreactivity (BHR) is still controversial. Thus the effects of CH on airway and tissue mechanics separately and changes in lung responsiveness to methacholine (MCh) were investigated. To clarify the mechanisms, mechanical changes were related to end-expiratory lung volume (EELV), in vivo results were compared with those in vitro, and lung histology was assessed. EELV was measured plethysmographically in two groups of rats exposed to 21 days of CH (11% O2) or to normoxia. Total respiratory impedance was measured under baseline conditions and following intravenous MCh challenges (2–18 μg·kg−1·min−1). The lungs were then excised and perfused, and the pulmonary input impedance was measured, while MCh provocations were repeated under a pulmonary capillary pressure of 5, 10, and 15 mmHg. Airway resistance, tissue damping, and elastance were extracted from the respiratory impedance and pulmonary input impedance spectra. The increases in EELV following CH were associated with decreases in airway resistance, whereas tissue damping and elastance remained unaffected. CH led to the development of severe BHR to MCh (206 ± 30 vs. 95 ± 24%, P < 0.001), which was not detectable when the same lungs were studied in vitro at any pulmonary capillary pressure levels maintained. Histology revealed pulmonary arterial vascular remodeling with overexpression of α-smooth muscle actin antibody in the bronchial wall. These findings suggest that, despite the counterbalancing effect of the increased EELV, BHR develops following CH, only in the presence of intact autonomous nervous system. Thus neural control plays a major role in the changes in the basal lung mechanics and responsiveness following CH.

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Groeben, Harald, Beatrix Schäfer, Goran Pavlakovic, Marie-Theres Silvanus i Juergen Peters. "Lung Function under High Thoracic Segmental Epidural Anesthesia with Ropivacaine or Bupivacaine in Patients with Severe Obstructive Pulmonary Disease Undergoing Breast Surgery". Anesthesiology 96, nr 3 (1.03.2002): 536–41. http://dx.doi.org/10.1097/00000542-200203000-00005.

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Background Because general anesthesia with tracheal intubation can elicit life-threatening bronchospasm in patients with bronchial hyperreactivity, epidural anesthesia is often preferred. However, segmental high thoracic epidural anesthesia (sTEA) causes pulmonary sympathetic and respiratory motor blockade. Whether it can be safely used for chest wall surgery as a primary anesthetic technique in patients with chronic obstructive pulmonary disease or asthma is unclear. Furthermore, ropivacaine supposedly evokes less motor blockade than bupivacaine and might minimize side effects. To test the feasibility of the technique and the hypotheses that (1) sTEA with ropivacaine or bupivacaine does not change lung function and (2) there is no difference between sTEA with ropivacaine or bupivacaine, the authors studied 20 patients with severe chronic obstructive pulmonary disease (forced expiratory volume in 1 s [FEV1] = 52.1 +/- 17.3% of predicted [mean +/- SD]) or asthma who were undergoing breast surgery. Methods In a double-blind, randomized fashion, sTEA was performed with 6.6 +/- 0.5 ml of either ropivacaine, 0.75% (n = 10), or bupivacaine, 0.75% (n = 10). FEV1, vital capacity, FEV1 over vital capacity, spread of analgesia (pin prick), hand and foot skin temperatures, mean arterial pressure, heart rate, and local anesthetic plasma concentrations were measured with patients in the sitting and supine positions before and during sTEA. Results Segmental high thoracic epidural anesthesia (segmental spread C4-T8 [bupivacaine] and C5-T9 [ropivacaine]) significantly decreased FEV1 from 1.22 +/- 0.54 l (supine) to 1.09 +/- 0.56 l (ropivacaine) and from 1.23 +/- 0.49 l to 1.12 +/- 0.46 l (bupivacaine). In contrast, FEV1 over vital capacity increased from 64.6 +/- 13.5 to 68.2 +/- 14.5% (ropivacaine) and from 62.8 +/- 12.4 to 66.5 +/- 13.6% (bupivacaine). There was no difference between ropivacaine and bupivacaine. Skin temperatures increased significantly, whereas arterial pressure and heart rate significantly decreased indicating widespread sympathetic blockade. All 20 patients tolerated surgery well. Conclusions Despite sympathetic blockade, sTEA does not increase airway obstruction and evokes only a small decrease in FEV1 as a sign of mild respiratory motor blockade with no difference between ropivacaine and bupivacaine. Therefore, sTEA can be used in patients with severe chronic obstructive pulmonary disease and asthma undergoing chest wall surgery as an alternative technique to general anesthesia.

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Aravitska, M. G. "Effectiveness of Physical Therapy in the Correction of Respiratory System Dysfunction Signs in Women with Abdominal Obesity". Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 5, nr 5 (1.11.2020): 248–57. http://dx.doi.org/10.26693/jmbs05.05.248.

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Respiratory disorders in obesity occur even in the absence of bronchopulmonary pathology, and in their presence, an excess of adipose tissue worsens the prognosis of the disease. Obese people have a high risk of obstructive sleep apnea syndrome, hypoventilation syndrome, bronchial hyperreactivity, pneumonia, pulmonary hypertension. The purpose of the study was to determine the effectiveness of using physical therapy in the correction of signs of respiratory system dysfunction in women with abdominal obesity. Material and methods. The study involved 172 women with abdominal obesity of I-III degrees, diagnosed by body mass index and the ratio of waist and hip circumferences. According to the results of the definition of the rehabilitation (therapeutic) alliance, they were divided into two groups. The comparison group consisted of women with a low level of alliance that refused to actively participate in the program of weight loss. The main group consisted of women with a high level of alliance; they underwent a one-year correction program using nutritional modification, increased physical activity, lymphatic drainage, psychocorrection, and elements of respiratory physical therapy. The control group consisted of 32 women with normal body weight. Subjective state, dyspnea intensity, pulsоoximetry and spirometry parameters were studied. Results and discussion. We revealed the respiratory system dysfunction in women with abdominal obesity: subjective signs of impaired respiratory function, a decrease in arterial blood oxygenation, and a decrease in spirometry volumes. Their content and severity were proportional to the severity of obesity. Using respiratory therapy elements in the program of complex physical therapy aimed at reducing body weight let us normalize the studied parameters of the respiratory system function in women of the main group. The low level of the rehabilitation alliance of women in the comparison group led to unsatisfactory implementation of the recommendations provided and was associated with a lack of rehabilitation effect. Improvement in the state of the bronchopulmonary system in women with abdominal obesity is justified both by primary changes in the respiratory system – an increase in spirometry volumes and reserves, improved blood oxygenation, and indirectly – by an increase in the range of motion of the diaphragm, a decrease in the amount of visceral fat and general fitness, which is confirmed by the leveling of signs of restrictive and mixed respiratory failure. Conclusion. It is advisable to include the elements of respiratory rehabilitation in the programs for restoring the health of women with abdominal obesity

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Delannoy, E., A. Courtois, V. Freund-Michel, V. Leblais, R. Marthan i B. Muller. "Hypoxia-induced hyperreactivity of pulmonary arteries: role of cyclooxygenase-2, isoprostanes, and thromboxane receptors". Cardiovascular Research 85, nr 3 (26.08.2009): 582–92. http://dx.doi.org/10.1093/cvr/cvp292.

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Hiram, Roddy, Edmond Rizcallah, Chantal Sirois, Marco Sirois, Caroline Morin, Samuel Fortin i Eric Rousseau. "Resolvin D1 reverses reactivity and Ca2+ sensitivity induced by ET-1, TNF-α, and IL-6 in the human pulmonary artery". American Journal of Physiology-Heart and Circulatory Physiology 307, nr 11 (1.12.2014): H1547—H1558. http://dx.doi.org/10.1152/ajpheart.00452.2014.

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Pulmonary hypertension (PH) is a rare and progressive disease characterized by an inflammatory status and vessel wall remodeling, resulting in increased pulmonary artery resistance. During the last decade, treatments have been proposed; most of them target the endothelial pathways that stimulate smooth muscle cell relaxation. However, PH remains associated with significant morbidity. We hypothesized that inflammation plays a crucial role in the severity of the abnormal vasoconstriction in PH. The goal of this study was to assess the effects of resolvin D1 (RvD1), a potent anti-inflammatory agent, on the pharmacological reactivity of human pulmonary arteries (HPAs) via an in vitro model of induced hyperreactivity. The effects of RvD1 and monoacylglyceride compounds were measured on contractile activity and Ca2+ sensitivity developed by HPAs that had been pretreated (or not) under proinflammatory conditions with either 10 ng/ml TNF-α or 10 ng/ml IL-6 or under hyperreactive conditions with 5 nM endothelin-1. The results demonstrated that, compared with controls, 24-h pretreatment with TNF-α, IL-6, or endothelin-1 increased reactivity and Ca2+ sensitivity of HPAs as revealed by agonist challenges with 80 mM KCl, 1 μM serotonin (5-hydroxytryptamine), 30 nM U-46619, and 1 μM phorbol 12,13-dibutyrate. However, 300 nM RvD1 as well as 1 μM monoacylglyceride-docosapentaenoic acid monoglyceride strongly reversed the overresponsiveness induced by both proinflammatory and hyperreactive treatments. In pretreated pulmonary artery smooth muscle cells, Western blot analyses revealed that RvD1 treatment decreased the phosphorylation level of CPI-17 and expression of transmembrane protein member 16A while increasing the detection of G protein-coupled receptor 32. The present data demonstrate that RvD1, a trihydroxylated docosahexaenoic acid derivative, decreases induced overreactivity in HPAs via a reduction in CPI-17 phosphorylation and transmembrane protein member 16A expression.

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Navarrete, Jessica Ariatna Carreto, Estanislao Antonio Calixto, David Sandoval Sánchez, Johan Mendoza Alva, Alejandro Daniel Huerta Carranza, Yunelly Paola Sarmiento Sosa, Karla Ruth Galindo Meza i in. "Aseptic Vegetation in Pulmonary Artery Valve, Finding in a Patient with Systemic Lupus Erythematosus. Case report". International Journal Of Medical Science And Clinical Research Studies 03, nr 02 (21.02.2023). http://dx.doi.org/10.47191/ijmscrs/v3-i2-17.

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Systemic lupus erythematosus (SLE) is an entity that promotes the formation of autoantibodies that trigger immune complexes that damage various organs of the body. Worldwide, SLE has a prevalence of 13-7000 per 100,000 people and leads to a high mortality from cardiovascular diseases, as well as the risk of developing lupus nephritis (LN) in 60% of cases. We present the case of a 41-year-old patient with a history of recently diagnosed arterial hypertension and bronchial hyperreactivity of 20 years of evolution, admitted for 1 month of evolution with asthenia, myalgia, arthralgia and fever; she identifies malar erythematous dermatosis and systolic murmur in a pulmonary focus. When presenting with proteinuria, microhematuria and renal functional impairment, positive ANAs were performed, which is why it was classified as lupus nephropathy, and she needed to start hemodialysis. In the presence of the murmur, an echocardiogram was performed, which showed a pulmonary valve with a 1cm image of vegetation, causing moderate regurgitation. With the diagnosis of Libman-Sacks endocarditis, anticoagulant treatment, steroids, and mycophenolate were started, evolving to normal renal function.

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Huang, Yan-Zen, Ji-Chun Wu, Gui-Feng Lu, Hui-Bin Li, Su-Mei Lai, Yi-Chen Lin, Long-Xin Gui, James S. K. Sham, Mo-Jun Lin i Da-Cen Lin. "Pulmonary Hypertension Induces Serotonin Hyperreactivity and Metabolic Reprogramming in Coronary Arteries via NOX1/4-TRPM2 Signaling Pathway". Hypertension, 4.01.2024. http://dx.doi.org/10.1161/hypertensionaha.123.21345.

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BACKGROUND: Clinical evidence revealed abnormal prevalence of coronary artery (CA) disease in patients with pulmonary hypertension (PH). The mechanistic connection between PH and CA disease is unclear. Serotonin (5-hydroxytryptamine), reactive oxygen species, and Ca 2+ signaling have been implicated in both PH and CA disease. Our recent study indicates that NOXs (NADPH oxidases) and TRPM2 (transient receptor potential cation channel subfamily M member 2) are key components of their interplay. We hypothesize that activation of the NOX-TRPM2 pathway facilitates the remodeling of CA in PH. METHODS: Left and right CAs from chronic hypoxia and monocrotaline-induced PH rats were collected to study vascular reactivity, gene expression, metabolism, and mitochondrial function. Inhibitors or specific siRNA were used to examine the pathological functions of NOX1/4-TRPM2 in CA smooth muscle cells. RESULTS: Significant CA remodeling and 5-hydroxytryptamine hyperreactivity in the right CA were observed in PH rats. NOX1/4-mediated reactive oxygen species production coupled with TRPM2-mediated Ca 2+ influx contributed to 5-hydroxytryptamine hyperresponsiveness. CA smooth muscle cells from chronic hypoxia-PH rats exhibited increased proliferation, migration, apoptosis, and metabolic reprogramming in an NOX1/4-TRPM2–dependent manner. Furthermore, the NOX1/4-TRPM2 pathway participated in mitochondrial dysfunction, involving mitochondrial DNA damage, reactive oxygen species production, elevated mitochondrial membrane potential, mitochondrial Ca 2+ accumulation, and mitochondrial fission. In vivo knockdown of NOX1/4 alleviated PH and suppressed CA remodeling in chronic hypoxia rats. CONCLUSIONS: PH triggers an increase in 5-hydroxytryptamine reactivity in the right CA and provokes metabolic reprogramming and mitochondrial disruption in CA smooth muscle cells via NOX1/4-TRPM2 activation. This signaling pathway may play an important role in CA remodeling and CA disease in PH.

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